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To the Editor:-Dilutional acidosis is an interesting concept but has not been clearly defined clinically. Mathes' et al. [1 ] and previous case reports [2,3 ] of metabolic acidosis secondary to the administration of large amount of normal saline have an additional feature in common, namely hyperchloremia. As a general rule, hyperchloremia is associated with metabolic acidosis and hypochloremia with metabolic alkalosis. In all these case reports, hyperchloremia may have caused the metabolic acidosis rather than by the dilution of serum bicarbonate. High chloride load as the cause of hyperchloremic metabolic acidosis has recently been suggested in anesthetic literature. [4 ]

How does a change in chloride concentration bring about such profound alteration in acid-base equilibrium? The answer to this question is not obvious when analyzed using the Henderson-Hasselbalch equation. However, it can be explained by Stewart's method of analysis of quantitative acid-base chemistry. [5 ] To understand and apply Stewart's approach to acid-base analysis and management requires a shift in the way we think and understand acid-base problems. Fencl and Leith [6 ] recently reviewed Stewart's quantitative approach to acid-base chemistry and summarized that “Stewart's approach shows the way to understanding and mathematical modeling of biological fluids as physico-chemical systems. It provides a basis for quantitative analysis and rational manipulation of acid-base state, in vivo and in vitro, and it challenges current interpretations of compartmentalized acid-base exchanges across biological membranes.”

According to Stewart, in a solution containing strong electrolytes, the difference in the sum of the positive charges and that of the negative charges carried by the strong ions, referred to as strong ion difference (SID), is one of the major determinants of hydrogen ion concentration. It is the net unbalanced positive charge on the strong ions present in the solution that is balanced by the net charge on all other weak ions. In normal plasma, SID has a numerical value of about 40. Lower values of SID lead to metabolic acidosis, and higher values lead to metabolic alkalosis. In Mathes' case report, the high chloride load may have caused a reduction in the SID, which resulted in the metabolic acidosis.

One of the interesting questions resulting from Stewart's approach relates to how sodium bicarbonate corrects the metabolic acidosis. The metabolic acidosis may be corrected not so much by its bicarbonate content but by its sodium content. The increased sodium concentration resulting from bicarbonate therapy corrects the reduced SID toward normal, thereby correcting the acidosis. According to Stewart, bicarbonate is a dependent variable and therefore cannot bring about a change in another dependent variable like hydrogen ion concentration.

In conclusion, we believe that hyperchloremia caused the metabolic acidosis by altering the SID, and we do not believe that dilution of bicarbonate is a likely cause.